Cerebral blood flow and systemic hemodynamics during exposure to 2 kPa CO2-300 kPa O2 in rats

Bergø, G. W.; Tyssebotn, I

doi:10.1152/jappl.1995.78.6.2100

Cited by 16 publications

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“…Hyperoxia increases systemic vascular resistance, reduces cardiac output, and paradoxically reduces whole body O 2 consumption,44 reducing slightly the adenine nucleotide pool 45. Hyperbaric hyperoxia causes a decline in heart rate and cardiac output, whereas blood pressure increases, with depression of capillary blood flow 46. O 2 delivery is unchanged by hyperoxia at low hyperbaric levels or at eubaria,47 supporting a vascular, not a parenchymal effect of O 2 in explaining our findings.…”

Section: Discussionsupporting

confidence: 53%

Eubaric hyperoxemia and experimental cerebral infarction

Flynn

Auer

2002

Annals of Neurology

101

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We explore three questions concerning arterial hyperoxygenation and focal ischemia. (1) Does greater benefit accrue with higher levels of arterial hyperoxemia? (2) Is the net effect of continuous (intraischemic plus postischemic) oxygen therapy toxic, or beneficial to middle cerebral artery infarction? (3) In view of free radical theories of reperfusion injury, does hyperoxia isolated to the reperfusion period damage tissue? Rats subjected to transient, focal, normothermic, normoglycemic ischemia were assessed at 2 weeks' survival. Arterial hyperoxygenation from 98.9 +/- 4.0 to 312.2 +/- 48.4mm Hg during ischemia improved (p < 0.05) neurological function, as did isolated reperfusion hyperoxemia, but treatment with continuous hyperoxemia both during and after ischemia yielded greatest benefit (p < 0.001). Cortical infarcts constituted 6.5 +/- 1.8% of the hemisphere at normoxia, but 2.3 +/- 0.9% at hyperoxic levels (p < 0.01). Hyperoxia isolated to the reperfusion period also reduced cortical necrosis, from 6.5% to 2.7 +/- 1.2%. However, continuous intraischemic and reperfusion hyperoxemia led to only 0.2 +/- 0.1% cortical necrosis (p = 0.0005). Increasing the degree of hyperoxemia did not augment the benefit. We conclude that (1) eubaric hyperoxemia improves neurological and neuropathological outcome, (2) continuous oxygen therapy offers the greatest benefit, and (3) reperfusion hyperoxemia is beneficial. The findings should allay clinical concerns regarding oxygen-induced reperfusion injury, and, by obviating hyperbaric chambers, encourage clinical trials studying arterial hyperoxemia in treating stroke.

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Section: Discussionsupporting

confidence: 53%

Eubaric hyperoxemia and experimental cerebral infarction

Flynn

Auer

2002

Annals of Neurology

101

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“…Although the overall effect of HBO is to lower CBF, prior to the development of HBO-induced seizures, there is a significant increase in CBF [52, 53]. This increase has been causally linked to the development of seizures as vasodilation through exposure to CO 2 decreases seizure latency in HBO exposed animals [54]. Also, vasodilatory nitric oxide levels have been found to be increased by HBO [53], and inhibitors of nitric oxide synthase increase seizure latency and attenuate increases in CBF [53, 55].…”

Section: Mechanism Of Action Of Hbomentioning

confidence: 99%

Hyperbaric Oxygen Therapy of Cerebral Ischemia

Helms

Whelan

Torbey³

2005

Cerebrovasc Dis

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Background: Hyperbaric oxygen (HBO) therapy of cerebral ischemia has been evaluated in a number of human and animal studies; however, there is presently no consensus on its efficacy. Methods: We present a review of animal and human studies on HBO therapy of cerebral ischemia as well as present potential mechanisms of action of HBO. Results: Animal studies of HBO have shown promise by reducing infarct size and improving neurologic outcome. HBO has also been shown to inhibit inflammation and apoptosis after cerebral ischemia. Early reports in humans also suggested benefit in stroke patients treated with HBO. Recent randomized, controlled human studies, however, have not shown benefit, although all were limited by small sample size. Important differences between animal and human studies suggest HBO might be more effective in stroke within the first few hours and at a pressure of 2–3 ATA. Conclusions: The clinical usefulness of HBO in the treatment of cerebral ischemia is not yet certain. Attention to emerging pathophysiologic data should be taken into consideration in design of any future clinical trials of HBO in acute ischemic stroke.

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“…However there is no information on the circulatory responses in dierent organs to a combined O 2 -CO 2 exposure, except for our recent demonstration of the increase in regional cerebral blood¯ows (Bergù and Tyssebotn 1995a). Theoretically, adding CO 2 to the hyperoxic breathing atmosphere might have unfavorable eects in addition to those eects caused by the O 2 itself, for example, in rats excess CO 2 potentiates the toxic eect of HBO, by reducing the latency to seizures (Kafka et al 1986;Bergù and Tyssebotn 1995a).…”

Section: Introductionmentioning

confidence: 95%

“…This work con®rms previous studies (Lambertsen 1978;Kafka et al 1986) that demonstrated a reduced O 2 tolerance in hypercapnic animals. The lowered seizure-threshold may be due to an increased production of O 2 radicals due to the high oxygen tension (Bergù and Tyssebotn 1995a) or altered cellular metabolic responses to changes in arterial pH and P a CO 2 . The present study supports the hypothesis that cerebral vasoconstriction during HBO exposure is a protective mechanism that delays the onset of O 2 induced convulsions (Donald 1947;Lambertsen 1978;Kafka et al 1986) in conscious animals and humans.…”

Section: Evaluation Of the Experimental Proceduresmentioning

confidence: 99%

Cardiovascular effects of hyperbaric oxygen with and without addition of carbon dioxide

Bergø¹,

Tyssebotn²

1999

Eur J Appl Physiol

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It is commonly believed that during hyperbaric oxygen (HBO) treatment, in spite of the vasoconstriction induced by the increased O2 content in the breathing gas, the elevated carrying capacity of O2 in the arterial blood results in augmented O2 delivery to tissues. The experiments described here tested the hypothesis that HBO treatment would be more efficient in delivering O2 to poorly perfused tissues if the vasoconstriction induced by elevated O2 could be abolished or attenuated by adding CO2 to the breathing gas. Organ blood flow (QOBF), systemic hemodynamics, and arterial blood gases were measured before, during and after exposure to either 300 kPa O2 (group 1) or 300 kPa O2 with 2 kPa CO2 (group 2), in awake, instrumented rats. During the HBO exposure the respiratory frequency (fb) fell (4 breaths x min(-1) x 100 kPa O2(-1)), with no changes in arterial CO2 tension (PaCO2), but when CO2 was added, fb and PaCO2 increased. The left ventricular pressure (LVP) and the systolic arterial pressure (SBP) increased. The maximum velocity of LVP (+dP/dt) rose linearly with LVP whether CO2 was added or not (r2 = 0.72 and 0.75 respectively). Similarly, the cardiac output (Qc) and heart rate (fc) fell, while the stroke volume (SV) was unaltered, independent of PaCO2. There was a general vasoconstriction in most organs in both groups, with the exception of the central nervous system (CNS), eyes, and respiratory muscles. HBO reduced the blood flow to the CNS by 30%, but this vasoconstriction was diminished or eliminated when CO2 was added. In group 2, the blood flow to the CNS rose linearly with increased PaCO2 and decreased pH. After decompression fc and SBP stayed high, while Qc returned to control values by reducing the SV; CNS blood flow remained markedly elevated in group 2, while in group 1, it returned to control levels. We conclude that the changes in fc, Qc, LVP, dP/dt, SBP and most QOBF values induced by HBO were not changed by hypercapnia. Blood flow to the CNS decreased during HBO treatment at a constant PaCO2. Hypercapnia prevented this decline. Elevated PaCO2 augmented O2 delivery to the CNS and eyes, but increased the susceptibility to O2 poisoning. A prolonged suppression of O2 supply to the CNS occurred during the HBO exposure and in air following the decompression in the absence of CO2. This suppression was offset by the addition of CO2 to the breathing gas.

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Cerebral blood flow and systemic hemodynamics during exposure to 2 kPa CO2-300 kPa O2 in rats

Cited by 16 publications

References 0 publications

Eubaric hyperoxemia and experimental cerebral infarction

Eubaric hyperoxemia and experimental cerebral infarction

Hyperbaric Oxygen Therapy of Cerebral Ischemia

Cardiovascular effects of hyperbaric oxygen with and without addition of carbon dioxide

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